Targeting the mitochondrial calcium uniporter to prevent ventricular arrhythmias in heart failure

The worldwide prevalence of heart failure (HF) continues to increase. 1 Ziaeian B. Fonarow G.C. Epidemiology and aetiology of heart failure. Nat Rev Cardiol. 2016; 13: 368-378 Crossref PubMed Scopus (769) Google Scholar A major challenge in the population with HF is the occurrence of ventricular arrhythmias, which are a major cause of morbidity and mortality in this patient population. 2 Husti Z. Varro A. Baczko I. Arrhythmogenic remodeling in the failing heart. Cells. 2021; 10: 3203 Crossref PubMed Scopus (5) Google Scholar The mechanisms leading to ventricular arrhythmias, such as ventricular tachycardia and ventricular fibrillation (VT/VF), remain incompletely understood. This represents a major clinical and scientific challenge. Addressing these areas could lead to improvements in quality of life and survival in patients with HF that are prone to sudden death due to the occurrence of ventricular arrhythmias. Stimulation of the mitochondrial calcium uniporter mitigates chronic heart failure–associated ventricular arrhythmia in miceHeart RhythmVol. 19Issue 10PreviewAn aberrant increase in the diastolic calcium concentration ([Ca2+]i) level is a hallmark of heart failure (HF) and the cause of delayed afterdepolarization and ventricular arrhythmia (VA). Although mitochondria play a role in regulating [Ca2+]i, whether they can compensate for the [Ca2+]i abnormality in ventricular myocytes is unknown. Full-Text PDF